
Eldad Tzahor
@Tzahore
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regenerative medicine, heart diseases, from basic to translation science. Prof. at Weizmann Institute of Science
Israel
Joined March 2014
I tried to describe my path from basic science to startups, from academia to industry and how to balance between the two efforts. Sometimes fun, often hard but i don't regret doing it. open link:
journals.biologists.com
ABSTRACT. Many developmental and stem cell biologists will be familiar with writing grant applications that discuss how their fundamental research findings might translate into discoveries that...
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My lab at @WeizmannScience was completely demolished by the Iranian missile a few days ago. This is hard and sad as nothing was left to save. We study heart regeneration and regenerative medicine. As such, we will regenerate, regrow and rebuild. The one thing that wasn't gone is
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Cardiac regeneration, @WeizmannScience #8400, my entrepreneurial efforts and more. in the Israeli Trailblazers Podcast with Jennifer Weissmann.
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While hard to see myself here. It was fun to chat with Jennifer about science and entrepreneurial paths I have taken in recent years and on @WeizmannScience and #8400.
In 2020 Israel grew unique muscle stem cells to make muscle fiber. Cultivated Steak? Pretty Cool Stuff Coming out of ISRAEL. @Tzahore
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Our paper plus the cover in @CellSystemsCP on cardiac fibrosis. A novel insight on these pathologies with some therapeutic solutions.
Our work made it to the cover of @CellSystemsCP! 🥳. Cold and hot fibrosis define clinically distinct cardiac pathologies. Check out our paper here: @UriAlonWeizmann @Tzahore @MiriAdler @WeizmannScience @HebrewU
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RT @BensimonBrito: Are you passionate about live-imaging microscopy? Do you have a special talent for working with iPSCs? Or are you simply….
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The story of our collaborative cardiac fibrosis paper with @UriAlonWeizmann, @MiyaraShoval, @MiriAdler and many more.
wis-wander.weizmann.ac.il
A collaborative study reveals two kinds of scarring, dubbed hot and cold, in injured heart tissue, suggesting that treatments must take the type of scar into account
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The story of our study:.
A collaborative study by @Tzahore @UriAlonWeizmann & @MiyaraShoval - published in Cell Systems - reveals two kinds of scarring, hot and cold, in injured heart tissue, suggesting that treatments must take the type of scar into account >> @Tzahor_Lab
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Last but not least, we thank @EladBassat and Jingkui Wang from the lab of @Tanaxolotl at @IMPvienna 🦾, Andrea Baehr, and Christian Kupatt @TU_Muenchen. Special thanks to the amazing Dr. Avi Mayo from the @UriAlonWeizmann team & Danielle Kimchi for original illustrations. End.
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Huge thanks to Daniel Haußler and Achim Kruger @TU_Muenchen, and the amazing @roramirezf94 and @JulioSaezRod @saezlab @UniHeidelberg @emblebi, and Tatjana Dorn and Alessandra Moretti from DZHK (13/).
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Hanna Bueno-Levy, Rachel Sarig from @Tzahor_Lab, Tali Shalit, Michael Gershovits and Eviatar Weizman from @WeizmannScience INCPM🦾🦾🦾 (12/).
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This work was made possible thanks to our amazing collaborators from around the world. Thank you to our lab members @JacobElkahal, Kfir Umansky @YalinDivinsky, @genzelinakh, @abingtonSA, @LinglingZhang12, @DavidKain17, Daria Lendengolts, @ZacharyPetrover (11/).
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In vivo, we demonstrate that inhibition of TIMP1 following myocardial infarction reduces myofibroblast proliferation and subsequent fibrosis. (10/)
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We demonstrate that TIMP1 acts as a growth factor for cardiac myofibroblasts derived from either mouse or non-human-primate hearts. (9/)
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Using scRNAseq and NicheNet analyses we identified TIMP1 as a key cardiac myofibroblast autocrine growth factor following myocardial infarction (8/)
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Our theoretical model revealed a vulnerability of ❄️cold fibrosis: the myofibroblast autocrine growth factor loop. (7/)
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We show that❄️cold fibrosis following myocardial infarction is conserved in mice, pigs, and humans (6/)
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Conversely, chronic cardiac injury, such as heart failure induced by ventricular pressure overload, results in 🔥 hot fibrosis- a state controlled by both myofibroblasts and macrophages (5/)
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We demonstrate that myocardial infarction results in ❄️ cold fibrosis- a state dominated by myofibroblasts. (4/)
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